Cardiac troponin I (cTnI) is used in human and veterinary medicine as a specific and sensitive marker for myocardial injury. In human cardiac disease, cTnI is shown to have predictive value for mortality. cTnI belongs to the troponin complex. In myocardial injury, it is released into the circulation.

To investigate the use of cTnI to assess progression of disease and as prognostic indicator, we reviewed the records of 125 dogs presenting for cardiac evaluation to the Small Animal Teaching Hospital between July 2004 and March 2008, in which serum cTnI had been assayed. Physical examination, systolic blood pressure, electrocardiography, and echocardiography data were obtained from all animals. Cases were categorised into the following groups: 20 dogs presented with congestive heart failure (CHF), 33 had stable congenital or acquired cardiac disease prior to CHF, 19 had tachyarrhythmias, 29 had significant bradyarrhythmias requiring pacemaker implantation, 6 had pericardial effusion and 18 had no cardiac disease.

In all dogs, the median cTnI was 0.26 ng/mL, with interquartile range of <0.11 ng/mL to 0.64 ng/mL. Kruskal Wallis ANOVA on ranks showed significant differences in cTnI between the groups (p<0.0001) with markedly elevated cTnI in dogs with CHF (median 1.12 ng/mL, range 0.27-180 ng/mL), bradyarrhythmias (median 0.50 ng/mL, range 0.05-180 ng/mL) and pericardial effusion (median 0.53 ng/mL, range 0.18-5.0 ng/mL).

Kaplan Meier survival analysis showed that dogs with cTnI < 1 ng/mL had median survival time of 1 year, compared with dogs with cTnI > 1 ng/mL surviving 3 months. Four animals with a median cTnI of 1.76 ng/mL (0.65-16.8 ng/mL) died within one week. Ninety animals are still alive with a median follow-up time of 11 months (range 0.5-44 months) and a median cTnI of 0.21 ng/mL (0.01-180 ng/mL). Dogs survived more than 1 year (n = 38), 2 years (n = 14) and 3 years (n = 5) had a median troponin of 0.18 ng/mL, 0.07 ng/mL and 0.05 ng/mL, respectively.

Repeat sampling after 10 days-2 years revealed no significant reduction in cTnI (p=0.08). Most dogs (70%) had cTnI remaining higher than the reference range suggesting ongoing cardiomyocyte injury. Animals with stable elevated or increasing cTnI levels at repeat sampling died within 2 months.

This study showed that cTnI is helpful to assess severity, disease progression and prognosis in cardiac patients. Repeat sampling is useful to evaluate progression and control of disease.